Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
 11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of beta 1 (very late activation antigens, VLA 1-6) and beta 2 integrins (leukocyte adhesion molecules [Leu-CAM]) in cell suspensions from the peripheral blood of 70 patients with B-cell chronic lymphocytic leukemia (B-CLL), 15 patients with leukemic lymphocytic lymphoma of intermediate differentiation (IDL), as well as from the lymph nodes of 20 patients with low/intermediate-grade non-Hodgkin's lymphoma (NHL) was studied with the aim of characterizing their adhesive phenotype and evaluating its relationship to clinical behavior. CD11a(LFA-1) was more expressed in NHL and IDL than in B-CLL (P = .047), although it was demonstrable in 74.2% of cases; CD11c was more expressed in B-CLL (P less than .0001), and its expression was preserved in almost all of the cases of small lymphocytic lymphoma. In NHL patients, including the cases of IDL, VLA-3 expression was observable in 8 of 35 cases (although always at a low level of intensity), while VLA-4 was almost constantly expressed in a way that was similar to its expression in control normal B cells. On the contrary, in B-CLL patients, VLA-3 was expressed (prevalently at high levels) in 87.1% of cases and VLA-4 only in 37.1%. No correlation was found between adhesion molecule patterns and the clinical features of the diseases. The biofunctional significance of the imbalance of VLA-3 and VLA-4 expression in B-CLL is not easy to explain, but it has undoubted intrinsic value as an additional marker for distinguishing B-CLL from, in particular, those B-cell neoplasms (such as IDL) that share many of the immunocytomorphologic characteristics and the putative normal counterpart (the mantle zone) of B-CLL.
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PMID:Differential expression of very late activation antigen-3 (VLA-3)/VLA-4 in B-cell non-Hodgkin lymphoma and B-cell chronic lymphocytic leukemia. 158 17

To investigate whether the lymphocyte homing receptor (LHR), an adhesion molecule believed to play an important role in the control of normal lymphocyte circulation, influences the spread of non-Hodgkin's lymphoma (NHL), expression of LHR was examined in 107 NHL of various histologic and immunophenotypic subclasses. This analysis revealed that whereas NHL with a putative derivation from recirculating mature T and B lymphocytes almost invariably express high levels of LHR, those akin to sessile mature or immature lymphocytes tend to express lower levels of LHR. Furthermore, in a survey among diffuse large-cell lymphomas of the B-lineage, the tumors of 11 of 13 patients with stage III/IV disease expressed moderate to high levels of LHR, whereas only two of 17 patients with stage I/II disease had tumors that did so. These findings suggest that LHR is involved in the dissemination of NHL.
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PMID:Expression of lymphocyte homing receptor as a mechanism of dissemination in non-Hodgkin's lymphoma. 264 48

Local tumor growth has been reported after subcutaneous and intraperitoneal injection of Hodgkin's disease (HD) derived cell lines into different immunodeficient mouse strains. An animal model with disseminated growth of tumor cells would be useful for studying the in vivo biology of HD cells as well as for preclinical testing of new therapeutic regimens. For this purpose the HD-derived cell lines L540, L540cy, L428, and KM-H2 were injected intravenously into SCID mice. In contrast to L428 and KM-H2, widespread neoplasia occurred after a period of four to six weeks following injection of L540 and the subline L540cy. Lymph nodes were found to be the preferred site of tumor growth. CD30 surface antigen expression on Hodgkin cells and the karyotype of the tumor cells were preserved in the animal host. Thus, to a large extent, the SCID mouse model mimics the dissemination pattern of Hodgkin's disease in man. To evaluate the role of adhesion molecule expression in the dissemination of HD-derived cell lines, CD44 and members of the immunoglobulin, integrin, selectin, and Fc receptor families were quantified by flow cytometry. CD30 expression was also measured. Although CD44 expression has been correlated with dissemination in non-Hodgkin's lymphoma (NHL), this was not the case in the Hodgkin's SCID mouse model. CD44 was not expressed on the disseminating cell lines L540 and L540cy but was expressed in the nondisseminating lines L428 and KM-H2.
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PMID:Disseminated growth of Hodgkin's-derived cell lines L540 and L540cy in immune-deficient SCID mice. 751 37

Variants of the CD44 cell-surface adhesion molecule include additional sequences encoded by combinations of exons from the membrane proximal domain (exons 6-14). Preliminary studies suggest that these additional variable membrane proximal sequences may alter the ligand specificity, glycosylation, and biologic function of CD44. In earlier studies, we found that primary extranodal and widely disseminated aggressive non-Hodgkin's lymphomas (NHLs) and normal activated B cells expressed a directly spliced exon 10-containing variant (CD44ex10), whereas normal resting B cells expressed larger exon 10-containing variants (CD44ex10-14 and CD44ex7-14). To obtain additional information regarding the function of exon 10-containing CD44 variants in aggressive NHL, we generated aggressive NHL transfectants that expressed CD44ex10, CD44ex10-14, CD44ex7-14, the standard CD44 isoform (CD44H), or vector alone, and evaluated the local tumorogenicity, aggregation, and metastatic potential of these transfectants. CD44ex10 aggressive NHL transfectants were more likely to cause local tumor formation in nude mice than transfectants expressing the larger exon 10-containing variants, CD44H, or vector alone. In addition, cell suspensions derived from CD44ex10 local tumors exhibited far greater homotypic aggregation than those obtained from other CD44 or vector-only local tumors. In nude mice that received CD44ex10 transfectants, distant metastases were also significantly more likely to develop than in animals that were given either the CD44ex10-14, CD44ex7-14, CD44H, or vector-only transfectants. These data provide the first evidence that the directly spliced exon 10-containing CD44 variant (CD44ex10) has a unique biologic function in aggressive NHL.
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PMID:A directly spliced exon 10-containing CD44 variant promotes the metastasis and homotypic aggregation of aggressive non-Hodgkin's lymphoma. 959 77

Serum levels and leukemic cell-tumor tissue expression of intracellular adhesion molecule-1 (ICAM-1/CD 54) were detected in 54 children with acute leukemia and malignant lymphoma. Serum samples were obtained from all patients before treatment and after cessation of the therapy from malignant lymphoma cases and during remission from leukemic patients. Twelve age-matched healthy children were included as a control group. The serum ICAM-1 levels were significantly higher in patients with acute lymphoblastic leukemia (ALL) or Hodgkin's disease (HD) than those in the control group (median values: 350.9, 286.4, and 138.4 ng/mL, respectively; P < .01 in each comparison). However, there were no significant differences concerning serum ICAM-1 levels between the control group and each of the acute myeloid leukemia (AML), non-Hodgkin's lymphoma (NHL), and Burkitt's lymphoma (BL) case groups (median values: 235.7, 222.7, 195.9, and 138.4 ng/mL, respectively; P > .05 in each comparison). Moreover, serum soluble ICAM-1 levels significantly declined in ALL or HD patients who were in complete remission (median values: 185.0 and 145.4 ng/mL, respectively; P < .05 in each comparison). In HD patients high levels of serum ICAM-1 could be correlated with high ESR (P < .01), whereas no statistically significant difference could be found when serum ICAM-1 titers were compared with stages, B symptoms, and histological subgroups, probably because of the inadequate number of patients in each group. Expression of ICAM-1 was mainly attributed to lymphocytes, vessels, and weakly to Hodgkin's cells, and this was significantly high in patients who were in advanced stages of disease. High serum sICAM-1 level was also associated with poor outcome and survival. Determination of serum level and/or tumor tissue expression of ICAM-1 in HD and ALL might represent an additional, but probably not independent, disease-associated marker to be used in the evaluation and/or monitoring of treatment response in patients with HD and ALL.
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PMID:Serum levels and differential expression of intercellular adhesion molecule-1 in childhood leukemia and malignant lymphoma: prognostic importance and relationship with survival. 1010 Feb 75

Lymphoid organ development and inflammation have previously been considered as distinct mechanistically and functionally. In recent years, it has been realized that these phenomena have much in common. This insight has been gained from the recognition that cytokines of the lymphotoxin (LT)/tumor necrosis factor (TNF) family are involved in both processes. The members of the family, LT-alpha, LT-beta, and TNF-alpha, and their multiple receptors participate combinatorially in lymphoid organ development and chronic inflammation. When inflammation that arises in microbial infection or autoimmune disease becomes chronic, it can take on the appearance of organized lymphoid tissue and has been called a tertiary lymphoid organ. Data with transgenic and knockout mice suggest that the process is cytokine-mediated and could be called "lymphoid neo-organogenesis." LT as LT-alpha3 and LT-alpha1beta2 plays a key role in these processes. Data obtained in vitro in an endothelial cell line and in vivo in transgenic and knockout mice indicate that LT influences these events through induction of adhesion molecules such as E-selectin adhesion molecule (ELAM), vascular cell adhesion molecule (VCAM), intercellular adhesion molecule (ICAM), mucosal addressin cellular adhesion molecule (MAdCAM), and peripheral node addressin (PNAd), and chemokines.
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PMID:Lymphoid neo-organogenesis: lymphotoxin's role in inflammation and development. 1049 67

Tumor-infiltrating CD8+ T-lymphocytes (T-TILs) are thought to be relevant to immunosurveillance of several tumor types including B-cell non-Hodgkin's lymphoma. B- and T-lymphocyte interactions via cellular adhesion molecules (CAMs), recognition molecules (HLAs), and costimulatory molecules (CSMs) are necessary for optimal antigen-specific T-cell activation to occur and may be important in generating effective host T-TIL responses. We previously found that low T-TIL response (CD8+ T cells < 6%) correlates with statistically shorter relapse-free survival in patients with diffuse large-cell lymphoma (DLCL). We now extend our observations in 71 DLCL patients by analyzing malignant B-cell expression of the following molecules important in T-cell activation: (a) recognition molecules [MHC I (MAS and MCA) and MHC II (HLA-DR, -DP, -DQ)]; (b) CAMs [leukocyte function antigen 1 (CD11a and CD18) and intracellular adhesion molecule 1 (CD54)]; and (c) CSMs [B7.1 (CD80) and B7.2 (CD86)]. Eighteen patients (25%) had low a T-TIL response, and 53 patients (75%) had a high T-TIL response. Overall, expression of the MHC class H molecules HLA-DR and HLA-DQ was most conserved. The loss of B7.2 (P = 0.04), intracellular adhesion molecule 1 (P = 0.0004), MAS (P = 0.02), and HLA-DR (P = 0.0004) expression was significantly associated with decreased T-TIL response. In 100% of patients with low T-TIL responses, at least one HLA, CAM, or CSM was undetectable on the malignant B cells by immunohistochemical staining (mean number of molecules lost = 2.67). In contrast, 49% of patients with high T-TIL responses had no losses in HLA, CAM, or CSM expression (mean number of molecules lost = 0.89). The mean number of absent molecules (HLA, CAM, or CSM) was significantly associated with T-TIL response (P = 0.0001). We conclude that loss of HLA, CAM, or CSM expression on malignant B cells is associated with a poor host T-cell immune response. In addition, because patients with low T-TIL response had lost expression of multiple cellular adhesion, recognition, and costimulatory molecules, our results suggest that a combination of immunorestorative therapies may be required to generate effective antitumor T-cell responses in B-cell DLCL.
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PMID:Loss of B7.2 (CD86) and intracellular adhesion molecule 1 (CD54) expression is associated with decreased tumor-infiltrating T lymphocytes in diffuse B-cell large-cell lymphoma. 1105 Dec 36

The classification of CD5-negative/CD10-negative chronic B-cell leukemias (CD5-/CD10- CBL) can be problematic. Most of these cases may represent leukemic non-Hodgkin's lymphoma (NHL) other than B-cell chronic lymphocytic leukemia (BCLL); nonetheless, some investigators still advocate the term "CD5-negative BCLL." Because adhesion molecule (AdMol) expression patterns reflect the biology of lymphoid neoplasms, we studied a series of 106 B-cell lymphoproliferative disorders, including CD5+ BCLL (n = 56), NHL other than BCLL (n = 35), and CD5-/CD10- CBL (excluding hairy cell leukemia and prolymphocytic leukemia) with no prior history of NHL (n = 15) for expression of components of the very late antigen-4 complex (alpha4/beta1 integrin (CD49d/CD29)), components of the mucosal addressin-cell adhesion molecule receptor (alpha4(CD49d)/beta7 integrin), and L-selectin (CD62L). CD62L expression was significantly greater in CD5+ BCLL than in NHL (P < .001). Conversely, CD29, CD49d, and beta7-integrin expression were significantly greater in NHL than in CD5+ BCLL (P < .001 for each marker). These differences persisted when only blood and bone marrow samples were analyzed, with the exception of differences in CD62L expression, which approached, but did not reach, statistical significance (P = .08). The group of CD5-/CD10- CBL displayed an AdMol profile similar to NHL and was significantly different than CD5+ BCLL in expression of beta7 integrin, CD29, CD49d, and CD62L (P range < .001-.011). In summary, CD5-/CD10- CBL display an AdMol profile resembling NHL and significantly different from CD5+ BCLL, supporting the growing notion that "CD5-negative BCLL" generally represents leukemic NHL rather than a variant of true CD5+ BCLL.
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PMID:Adhesion molecule expression in CD5-negative/CD10-negative chronic B-cell leukemias: comparison with non-Hodgkin's lymphomas and CD5-positive B-cell chronic lymphocytic leukemia. 1117 97

CD22 is a 135-kd B-cell restricted sialoglycoprotein present in the cytoplasm of virtually all B-lineage cells but expressed on the B-cell surface only at mature stages of differentiation. In humans, the vast majority of IgM(+)IgD(+) B cells express cell-surface CD22, while in lymphoid tissues CD22 expression is high in follicular mantle and marginal zone B cells and weak in germinal center B cells. In B-cell malignancies, CD22 expression ranges from 60% to 80% depending on the histological type and on the assays used. The function of the CD22 molecule is uncertain, although recent studies have suggested roles for the molecule both as a component of the B-cell activation complex and as an adhesion molecule. CD22-deficient mice have a reduced number of mature B cells in the bone marrow and circulation; the B cells have a shorter lifespan and enhanced apoptosis, thus indicating a key role of this antigen in B-cell development/survival. After binding with its natural ligand(s) or antibodies, CD22 is rapidly internalized; this provides a potent costimulatory signal in primary B-cell and proapoptotic signals in neoplastic B cells. Preclinically CD22 has been shown to be an effective target for immunotherapy of B-cell malignancies using either "naked" or toxin-labeled or radiolabeled monoclonal antibodies. Clinical trials in patients with non-Hodgkin's lymphoma (NHL) (both indolent and aggressive disease) are now ongoing with a humanized naked anti-CD22 antibody (epratuzumab, Amgen Inc, thousand Oaks, CA and Immunomedics Inc, Morris Plains, NJ) used as single agent or in combination with other monclonal antibodies (ie, rituximab) and/or chemotherapy. Preliminary data from these studies showed these approaches to be effective and well-tolerated.
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PMID:CD22 as a target of passive immunotherapy. 1272 Jan 47

During murine embryogenesis, the formation of Peyer's patches (PPs) is initiated by CD45(+)CD4(+)CD3(-) lymphoid tissue inducers that trigger adhesion molecule expression and specific chemokine production from an organizing stromal cell population through ligation of the lymphotoxin-beta receptor. However, the steps involved in the development of lymph nodes (LNs) are less clear than those of PPs, and the characteristics of the organizing cells within the LN anlagen have yet to be documented. In this study, we show for the first time that the early anlage is bordered by an endothelial layer that retains a mixed lymphatic and blood vascular phenotype up to embryonic day 16.5. This in turn encompasses CD45(+)CD4(+)CD3(-) cells interspersed with ICAM-1/VCAM-1/mucosal addressin cell adhesion molecule-1, lymphotoxin-beta receptor-positive, chemokine-producing cells analogous to the organizing population previously observed in PPs. Moreover, these LN organizers also express the TNF family member, TRANCE. Lastly, we show that the ICAM-1/VCAM-1/mucosal addressin cell adhesion molecule-1 cells present in peripheral and mesenteric LN form two discrete populations expressing either intermediate or high levels of these adhesion molecules but that the former population is specifically reduced in PLN. These findings provide a possible explanation for the well-known differences in developmental requirements for nodes at peripheral or mesenteric locations.
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PMID:Presumptive lymph node organizers are differentially represented in developing mesenteric and peripheral nodes. 1532 55


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